Neonatal respiratory distress related to colonization with group B streptococci[unreadable] Lin, Ogbonna, Schneerson, and Robbins in collaboration with Troendle, Yergey, Curtis, and Levine.[unreadable] [unreadable] Despite the decrease in the incidence of early-onset group B streptococcal (GBS) disease due to widespread use of antibiotic prophylaxis during labor, GBS remains a leading cause of neonatal sepsis. [unreadable] [unreadable] Clinical features of early-onset GBS disease are similar to those of endotoxic shock, and respiratory distress is a prominent symptom. Respiratory distress may occur in newborns, without a known GBS infection. Studies on the effect of GBS on pulmonary hemodynamics in animal models showed that infusion of live or heat-killed GBS into sheep promptly induced pulmonary hypertension. Curtis and associates purified and identified phospholipids (cardiolipin and phosphatidylglycerol) from the GBS cell wall as pulmonary hypertensive compounds; infusion of either cardiolipin or phosphatidylglycerol into neonatal lambs caused pulmonary hypertension. Others have demonstrated that exposure of Streptococcus mutans to penicillin induces a 15-fold increase in phospholipid release from the organism. Penicillin is one of -lactam antibiotics which inhibit the normal assembly of peptidoglycan of bacterial cell wall.[unreadable] [unreadable] These findings raised the question whether exposure of GBS to penicillin or to other -lactam antibiotics in newborns and mothers induces a release of GBS phospholipids causing pulmonary hypertension respiratory distress in newborns. It is recommended that newborns infected with GBS or whose mothers carry GBS be treated with penicillin or its derivatives.[unreadable] [unreadable] Analysis of a data file of the NICHD multicenter GBS study found a possible association between GBS colonization, penicillin treatment and respiratory distress in neonates. The results of analyses showed that 8.8% of GBS colonized newborns who did not develop early-onset GBS disease had respiratory distress within 48 h after birth compared to 1-3% of non colonized newborns. Furthermore, colonized newborns of penicillintreated mothers were 2.62 times more likely to develop respiratory distress than those of GBS carrying but untreated mothers (95%CI:1.79-3.83).[unreadable] [unreadable] Although the effect of cardiolipin on pulmonary hypertension and of penicillin on phospholipid release from S. mutans support the role of GBS colonization and penicillin on respiratory distress in newborns, a proof of these associations requires assay of GBS phospholipids in serum samples of newborns with and without respiratory distress of GBS-colonized mothers, treated or untreated with penicillin or other -lactam antibiotics during labor. Such an assay is being developed in collaboration with Dr. Alfred Yergey. [unreadable] [unreadable] A prospective study aimed at relating serum GBS phospholipid levels to the occurrence of respiratory distress in newborns of GBS colonized mothers is underway in two U.S. academic centers Baylor College of Medicine, Houston, Texas and Childrens Hospital and Research Center Oakland, California. Our sample size estimate suggests a need for 1600 colonized mothers who are at least 32 weeks gestation at delivery. A semiquantitative culture is used to determine the degree of colonization in the mothers. Three groups of GBS colonized mothers are being assembled: untreated, -lactam antibiotic-treated, and treated with non- -lactam antibiotics. Maternal and cord blood samples are being collected for the cardiolipin assay. All newborns are monitored for signs of respiratory distress. Two groups of newborns are being assembled: with and without respiratory distress.